Antigen-presenting innate lymphoid cells orchestrate neuroinflammation

Citation

Verified title: Antigen-presenting innate lymphoid cells orchestrate neuroinflammation
Publication year: 2021
DOI: 10.1038/s41586-021-04136-4
Metadata source: crossref-doi (confidence: high)
Original local title: Antigen-presenting innate lymphoid cells orchestrate neuroinflammation

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page has been manually reviewed for the adaptive-immunity follow-up question, including model system, tissue compartment, immune-cell target, assay directness, and claim-level boundaries.
Required boundary: reusable claims should preserve species, tissue, disease model, and whether evidence is primary perturbation, human association, ex vivo function, lineage taxonomy, or review-level synthesis.

Source Type

primary mouse and human neuroinflammation ILC3 antigen-presentation study - Evidence profile: CNS-infiltrating inflammatory ILC3s, MHCII antigen presentation, myelin-specific T-cell restimulation, multiple-sclerosis-like disease, and human multiple sclerosis association. - Knowledge note status: source-reviewed evidence note for extrapulmonary ILC3-T-cell antigen-presentation context.

Evidence Profile

Overall confidence: high for source-specific CNS evidence that antigen-presenting inflammatory ILC3s can restimulate pathogenic T cells in neuroinflammation. - Evidence tags: #source/primary #species/mouse #species/human #tissue/CNS #cell/ILC3 #cell/T_cell #assay/flow #assay/in_vivo #assay/in_vitro #outcome/inflammation #axis/adaptive_immunity #axis/ILC_regulation #status/focused_crystallization - Primary biological axis: CNS-infiltrating ILC3s can act as antigen-presenting cells that promote myelin-specific T-cell responses in neuroinflammation.

Why It Matters Here

This source broadens the ILC3 antigen-presentation model beyond gut tolerance by showing a pathogenic T-cell restimulation branch in CNS inflammation.

Key Findings

In a mouse multiple-sclerosis-like model, inflammatory ILC3s infiltrated the CNS and localized near T cells.
These ILC3s functioned as antigen-presenting cells that restimulated myelin-specific T cells.
Antigen presentation by inflammatory ILC3s was required to promote T-cell responses and disease development in the reported model.
Human multiple sclerosis association supports relevance, but this is CNS rather than lung evidence.

Claim-Level Confidence

High confidence: inflammatory CNS ILC3s can promote pathogenic T-cell responses through antigen presentation in the reported system.
Medium-high confidence: ILC3 antigen presentation can be tolerogenic or inflammatory depending on tissue and activation state.
Low confidence: direct pulmonary extrapolation is not justified.

Methods and Context

Species/context: mouse neuroinflammation model with human multiple sclerosis association.
Compartment: CNS and circulation.
Assay directness: strong for CNS ILC3-T-cell interaction; indirect for lung.
Best wiki use: contrast with gut tolerogenic MHCII ILC3 pathways.

Caveats

Keep CNS context explicit.
Do not merge pathogenic CNS antigen presentation with gut tolerance without noting directionality.
Not direct lung disease evidence.

Contradiction and Supersession

Contradiction status: contrasts with gut ILC3-MHCII tolerance, showing context-dependent antigen-presentation outcomes.
Supersession status: not superseded.